Term
diabetes mellitus "sweet urine" |
|
Definition
- life-long disorder of CHO (carbohydrate) metabolism resulting fro deficiency of or resistance to available insulin & characterized by hyperglycemia
- growing epidemic: estimated 17 millioin people (6.2% of US population) have diabetes; each yr about 1 million age 20 yrs + are diagnosed
- prevalence of DM in the US is predicted to be 8.9% by 2025
- much of the increase in diabetes is linked to the rapid rise in obesity & decrase in physical activity; the risk of diabetes is estimated to increase 5-10% for each 2lb increase in weight
|
|
|
Term
|
Definition
- results from a cellular-mediated autoimmune destruction of the insulin-producing B-cells in the islets of Langerhands of the pancreas
- occurs in genetically susceptible people, is probably triggered by one or more environmental agents
- majority of pts have anutoimmune destruction of the pancreatic B-cells as the underlying cause, have an absolute requirement for insulin tharapy & will develop diabetic ketoacidosis (DKA) if not given insulin
- mainly occurs in kids & adolescents, but can occur at any age
- accounts for 5-10% of diabetes
- more prevalent in caucasians
|
|
|
Term
|
Definition
acute onset increased thirst (polydipsia) - due to increased osmolarity increased urination (polyuria) constant hunger (polyphagia) b/c starving cells weight loss despite increased appetite b/c starving cells n/v blurred vision (b/c retina & brain do not store glucose) extreme fatigue (b/c no energy) if not treated w/ insulin: DKA, diabetic coma, death |
|
|
Term
|
Definition
- insidious onset, occurring over many yers; as a result, diabetic microvascular complications may be present when the diagnosis is made & their frequency increases over time
- frequently undiagnosed for many yrs b/c hyperglycemia develops gradually & at earlier stages is not severe enough to produce clinical symptoms
- specific etiologies of DM type 2 = unknown; however, there is no autoimmune destruction of B-cells
- most frequently resuts from peripheral insulin resistance w/ relative rather than absolute insulin deficiency; at least intitially & often throughout their lifetime, these pts do not need insulin tx to survive
- prolonged, compensatory hyper-secretion of insulin may lead to B-cell "burn-out"
- typically occurs over age 40 in obese pts; most common in adults older than 55 yrs; increasing incidence in adolescents
- represents 90% of all pts w/ diabetes
|
|
|
Term
|
Definition
- classic: polyuria or nocturia, polydypsia, polyphagia, unexplained weight loss
- other symptoms: blurred vision, freqent UTIs & yeast infections, fatigue, dry or pruritic skin, numbness or tingling in the extremities (due to neuropathy)
|
|
|
Term
overview of blood glucose regulation |
|
Definition
- glucose in nec. for energy production
- brain, retina & gonads cannot store glucose; very dependent on blood glucose levels
- humanseat in intervals; w/o regulation our blood glucose levels would rise & fall throughout the day
- normal blood glucose level = 60-110 (worried below 40)
- hyperglycemia/hypoglycemia
- two main organs involved in blood glucose regulation: liver & pancreas
- liver is able to convert glucose to glycogen & store it
- pancreas releases 2 hormones, insulin & glucagon, from the islets of langerhans
|
|
|
Term
|
Definition
- 51 amino acid protein consisting of 2 polypeptide chaings connected by disulfide bonds
- only hormone capable of lowering blood glucose level
- affects the metabolixm of carbs, proteins, fats; helps regulate the expenditure of engery; lowers blood glucose levels by stimulation the gransport of glucose from the blood into cells; activates intracellular glucago - enzyme involved in the combining of glucose molecules into glycogen & subsequent intracellular storage of glycogen; controls gluconeogenesis - release of glucose from the liver cells into bloodstream & inhibits lipolysis (breakdown of fat into adipose tissue)
- in summary, insulin is responsible for:
- facilitating the passage of glucose into cells for energy
- suppressing excess production of glucose in liver
- suppressing breakdown of fat for energy
|
|
|
Term
DM type 2 insulin negative feedback loop |
|
Definition
insulin lowers the blood glucose by decreasing the release of glucose from the liver & increasing the utilization of glucose by muscle & fat cells hyperglycemia can result from 3 main defects where the loop will not be active: - excessive glucose production by the liver (insensitive to insulin)
- absent or impaired insulin production & secretion by the pancreas
- peripheral insulin resistance in the muscles
|
|
|
Term
pathophysiologic processes in DM type 1 |
|
Definition
- without insulin, glucose cannot enter adipose & muscle tissues, leading to elevated blood glucose levels (hyperglycemia)
- destruction of 80-90% of the B-cells occurs before hyperglycemia is observed
|
|
|
Term
pathophysiologic processes in DM type 2 |
|
Definition
- "silent killer" b/c pts feel fine w/ increased levels of glucose
- after ingestion of glucose, maintenance of normal glucose tolerance depends on 3 events that must occur in a tightly coordinated fashion:
- stim of insulin secretion
- insulin-mediated suppression on endogenous (primarily hepatic) glucose production
- insuline-mediated sim of gluose uptake by peripheral tissues, primarily muscle
|
|
|
Term
|
Definition
- to maintain blood glucose levels near normal
- to prevent acute complications (e.g. hypoglycemia, ketoacidosis)
- to prevent intermediate compliations (e.g. lipoatrophy, lipohypertrophy, limited joint mobility, growth failure)
- to prevent chronic complications (e.g. microvascular/macrovascular complications, retinopathy, nephropathy, neuropathy)
|
|
|
Term
|
Definition
hormone w/ a short life (5-7 min) & physiologic profile that requires rapid changes in conc (by several fold) in response to nutrient intake & other physiological stimuli like exercises discovered in 1921 at the University of Toronto & administered for the first time in Jan 1922 |
|
|
Term
pharmacotherapeutics of insulin therapy |
|
Definition
all pts w/ DM type 1 pts w/ DM type 2 not controlled by other forms of tx women w/ gestational diabetes uncontrolled by dietary therapy tx of DKA (diabetic ketoacidosis) frequently during active diseases in hospital b/c of stress to body degraded in GI tract if taken orally; admin. SC or IV (in urgent situations) |
|
|
Term
properties of insulin: species |
|
Definition
- animal insulin: isolated from beef & pork pancreas; pork more closely resembles human, differing by only one amino acid; most of these have been replaced by the human form
- human insulin: produced by special strain of E.coli that has been genetically altered to contain the gene for human insulin
- has less antigenicity than that of animal insulin; onset, peak & duration are slightly different than those of animal insulin so the pt's insulin should not be changed from one species to anohter on a random basis
- newly diagnosed diabetics should be on human insulin b/c of its lower incidence of insulin allergy, resistance & lipoatrophy
|
|
|
Term
properties of insulin: strength |
|
Definition
- insulin preparations vary in coc of insulin units in 1cc volume
- strength most frequently used is U-100 insulin, or 100U/cc - special bottles
- in insulin resistance, a rare condition in which daily insulin doses exceed 100 units, U-500 insulin may be used
- 1 unit of insulin = 20-25mg increase in glucose
|
|
|
Term
properties of insulin: purity |
|
Definition
- standard insulin may contain small amts of pro-insulin-like substance & other antigenic substance
- insulin labeled "highly purified" contain less than 10 PPM of antigenic substances & are recommended for persons w/ newly diagnosed diabetes, insulin allergy, insulin lipodystrophy, or when intermittent insulin therapy is required --> NOW, ALL ARE HIGHLY PURIFIED
- beef insulin are antigenic than pork, human insulin the least antigenic of al
|
|
|
Term
properties of insulin: type of action |
|
Definition
- all insulins are hypoglycemic, but they differ in:
- speed of effect (onset)
- time of greatest action (peak)
- how long they act (duration)
- mixture ratio of zinc protamine & other substances to insulin dtermines the rate of release & the onset, peak, and duration of action of a particular type of insulin preparation
|
|
|
Term
insulin preparations: ultra-rapid acting |
|
Definition
- insulin lispro (Humolog) / insulin aspart (Novolog)
- onset: 10-15min
- peak: 1/2 - 1 1/2 hrs
- duration: 3-5 hrs
- modified insulin analogues (amino acids in postions 28 & 29 reversed)
- absorbed more rapidly than human regular insulin after SQ injection
- if given IV< behaves as regular insulin
- used in external insulin pumps
|
|
|
Term
insulin preparations: rapid (short) acting |
|
Definition
- regular (R) insulin (Novolin R)
- most often used
- onset: 1/2-1 hr
- peak: 2-4 hrs (this is where we'd check for hypoglycemia)
- duration: 6-8 hrs
- usually given SC 30 min before meals
- only insulin prep suitable for IV admin & sliding scale
|
|
|
Term
insulin preparations: intermediate-acting |
|
Definition
- NPH (N) (Novolin N, Humulin N)
- neutral protamin hagedrom (Isophane insulin suspension); suspension of crystalline zinc insulin combined at neutral pH w/ pos charged protamine
- Lente (L)
- onset: 1-4 hrs
- peak: 6-12 hrs
- duration: 24 hrs
- rate of absorption is slowed by conjugating the insulin w/ protamine to form less soluble complex
- should be given SC never IV
- useful in tx of all forms of diabetes except diabeticketoacidosis or emergency hyperglycemia
- preparation is cloudy
|
|
|
Term
insulin preparations: long-acting |
|
Definition
- ultralente (U) (Humulin U)
- onset: 4-8 hrs
- peak: 16-18 hrs
- duration: 24-36 hrs
- given only SC
- glargine (G) (Lantus)
- duration = 24 hrs
- modified insulin analogue
- soluble in acidic media but form precipitate when injected SC (pH 7.4), allowing slow absorption over 24 hrs
- results in "peakless" once-a-day insulin that provides steady level throughout the day
- preparation is clear, colorless (do not mistake for regular insulin; IV injection neutralizes sustained-release properties)
- do not mix w/ other insulin preparations (change in pH, eliminates 24-hr duration)
|
|
|
Term
insulin preparations: pre-mixed |
|
Definition
- NPH & regular insulin mixed together in container
- 70/30 & 50/50
- onset: 30 min
- peak: 8-12 hrs
- duration: 16-24 hrs
|
|
|